Growth arrest of hormone-dependent mammary carcinomas was achieved by orally administered DBcAMP. Total- and bound-radioactivities were 2-fold higher in the tumors and mammary gland when (3H)DBcAMP was administered orally as compared to s.c. administration. Orally administered DBcAMP elicited the increase of cAMP-dependent protein kinase in the regressing mammary carcinomas. Studies of RNA-polymerase and in vitro translation of polyA RNA isolated from growing and regressing mammary carcinomas suggested the action of cAMP at the nuclear level in the inhibition of mammary carcinoma growth.